<p>Premature ovarian insufficiency (POI) not only affects fertility, but also has a profound impact on women’s general health, mental health and quality of life. This research was designed to explain the function and mechanism of wild-type and edited miR-483-5p in POI. Western blot analysis and RT-qPCR were utilized to evaluate gene expression. Human granulosa cell activities were assessed via CCK-8, colony formation, EdU and TUNEL assays. FSH, E2, and AMH levels were measured using ELISA. Commercially available kits were obtained to detect glucose uptake and ROS level. The targets of miRNAs were confirmed through dual-luciferase reporter assay. High editing level of miR-483-5p induced by ADAR1 enzyme was related to high FSH level and low E2, AMH levels in POI patients. Functionally, miR-483-5p restrained granulosa cell proliferation and elevated apoptosis. Interestingly, A-to-I RNA editing aggravated miR-483-5p effect on granulosa cell activity. In vivo experiment also demonstrated that edited and wild-type miR-483-5p exacerbated POI by regulating granulosa cell proliferation and apoptosis. Mechanically, A-to-I RNA editing alters the targets of miR-483-5p. And ed-miR-483-5p obtains novel target ESR2 and loses ELK1. Specifically, miR-483-5p promoted POI progression by intensifying ELK1-mediated oxidative stress. Edited miR-483-5p aggravated POI development by downregulating ESR2-mediated hormone synthesis and glycometabolism. A-to-I RNA editing reinforces the pathogenicity of miR-483-5p in POI by regulating hormone synthesis and glucose metabolic mechanism through altering its target ELK1 as ESR2.</p>